UVM Theses and Dissertations
Format:
Print
Author:
Otty, Robert H.
Dept./Program:
Medical Laboratory Science Program
Year:
2004
Degree:
M.S.
Abstract:
Introduction: Periodontal disease is the most common chronic, inflammatory disease in adults. Advanced periodontal disease can result in attachment loss and destruction of the gingiva, resulting in deepening periodontal pockets. Together with bone loss these factors can ultimately lead to tooth loss. A wide variety of cell types can be stimulated to produce cytokines, which ultimately initiate inflammation. IL-l and IL-8 are two important cytokines involved in inflammation. Both of these cytokines are produced early in infection and are involved in recruiting immune cells to the site of infection. Interestingly, IL-l and IL-8 can stimulate release of enzymes that may contribute to many aspects of the tissue destruction seen in periodontal disease. More than 400 species of bacteria may reside in the oral cavity. Several of these species have been grouped based on their tendency to be found together, and particular groups tend to be associated with health versus disease. The goal of this study was to investigate whether correlations exist between the presence of bacteria associated with periodontal disease, the clinical presentation and the presence of IL-l and IL-8.
Materials and Methods: Pre- and posttreatment samples were collected from a control cohort and a test cohort. Clinical assessment was made, subgingival plaque samples and gingival crevicular fluid samples were collected for bacterial and cytokine analysis, respectively. A slot blot DNA-DNA hybridization technique was used to test for the presence of our bacteria of interest. ELISAs were used to analyze gingival crevicular fluid samples for IL-l and IL-8. Results: The control and the test groups appear to respond differently to treatment with respect to IL-l levels, however there was no difference in IL-8 response. In the control group, but not the test group, the relative location of teeth made a significant difference in the concentration of IL-l and IL-8. The results of our bacterial analyses were not consistent with previous reports. Bacteria11eve1s were not correlated with cytokine levels, or pocket depth, but were strongly correlated with inflammation score. Also, IL-1 was not correlated with clinical presentations including inflammation score and pocket depth. While IL-8 levels were not correlated with pocket depth, they were slightly correlated with inflammation score, although not consistently.
Discussion: Relative ease of access for hygiene likely contributes to the different cytokine levels at different tooth locations observed in the control group. It seems likely that the lack of a difference in cytokine levels between tooth locations in the test group indicates that factors contributing to periodontal disease are evenly distributed throughout the oral cavity. The lack of correlations between bacterial leve1s and cytokine levels indicate that the bacteria present may not be the sole factor involved in determining the inflammatory response and that IL-l and IL-8 may not be most important mediators of the immune response to periodontal bacteria. That neither IL-l nor IL-8 is consistently correlated with clinical presentation shows that other cytokines may be more significant contributors to the inflammation seen in periodontal disease. Studies built upon this work may include further investigation of which cytokines are important in the immune response to periodontal bacteria and contribute most significantly to the clinica1 presentation in periodontal disease. We cannot rule out the influences that variability in sampling techniques between groups, and a lack of advanced periodontitis in the test group, may have had on our findings. Future study designs should normalize for variability in sample collections and include a wider spectrum of clinical presentations.
Materials and Methods: Pre- and posttreatment samples were collected from a control cohort and a test cohort. Clinical assessment was made, subgingival plaque samples and gingival crevicular fluid samples were collected for bacterial and cytokine analysis, respectively. A slot blot DNA-DNA hybridization technique was used to test for the presence of our bacteria of interest. ELISAs were used to analyze gingival crevicular fluid samples for IL-l and IL-8. Results: The control and the test groups appear to respond differently to treatment with respect to IL-l levels, however there was no difference in IL-8 response. In the control group, but not the test group, the relative location of teeth made a significant difference in the concentration of IL-l and IL-8. The results of our bacterial analyses were not consistent with previous reports. Bacteria11eve1s were not correlated with cytokine levels, or pocket depth, but were strongly correlated with inflammation score. Also, IL-1 was not correlated with clinical presentations including inflammation score and pocket depth. While IL-8 levels were not correlated with pocket depth, they were slightly correlated with inflammation score, although not consistently.
Discussion: Relative ease of access for hygiene likely contributes to the different cytokine levels at different tooth locations observed in the control group. It seems likely that the lack of a difference in cytokine levels between tooth locations in the test group indicates that factors contributing to periodontal disease are evenly distributed throughout the oral cavity. The lack of correlations between bacterial leve1s and cytokine levels indicate that the bacteria present may not be the sole factor involved in determining the inflammatory response and that IL-l and IL-8 may not be most important mediators of the immune response to periodontal bacteria. That neither IL-l nor IL-8 is consistently correlated with clinical presentation shows that other cytokines may be more significant contributors to the inflammation seen in periodontal disease. Studies built upon this work may include further investigation of which cytokines are important in the immune response to periodontal bacteria and contribute most significantly to the clinica1 presentation in periodontal disease. We cannot rule out the influences that variability in sampling techniques between groups, and a lack of advanced periodontitis in the test group, may have had on our findings. Future study designs should normalize for variability in sample collections and include a wider spectrum of clinical presentations.